The Molecular Biology of Cancer


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The majority of ovarian cancers are sporadic and arise from an accumulation of genetic damage Ovarian cancers are heterogeneous regarding histopathology and malignant potential; therefore, the characteristic patterns of molecular signature are also varied Sporadic high-grade serous adenocarcinoma is usually advanced at diagnosis and the prognosis of patients is poor.

Mucinous adenocarcinoma is usually diagnosed at an early stage of disease and characterized by mutations in K-RAS Randomized phase II studies of platinum-sensitive recurrent high-grade serous cancers both germline BRCA and sporadic showed that patients treated with a PARP inhibitor exhibited a significant improvement in PFS when compared with patients who were administered a placebo Lysophosphatidic acid, heparin-binding EGF HB-EGF and amphiregulin, have been reported to play pivotal roles in proliferation and dissemination of ovarian cancer , Yagi et al reported that inhibitory agents against HB-EGF, including CRM, were possible chemotherapeutic and chemosensitizing agents for ovarian cancer The clinical application of novel treatments which target these molecules is expected in the future.

Since it is challenging to treat advanced or recurrent cancers using conventional treatments, the development of novel and highly specific targets for therapy is required.

Molecular Biology of Cancer

An exponential growth in the collection of genomic and proteomic data in the past 20 years has provided major advances in understanding the molecular mechanisms of human cancer. This progress has resulted in the development of targeted therapies tailored to an individual molecular profile. Recent advances in biochemical engineering should contribute to major evolution in diagnosis and treatment of human cancer.

N Engl J Med. Lancet Oncol. Mok TS: Personalized medicine in lung cancer: What we need to know. Nat Rev Clin Oncol.


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Int J Biochem Cell Biol. Bishayee A, Beguinot L and Bishayee S: Phosphorylation of tyrosine , , and is required for conformational change of the human epidermal growth factor receptor c-terminal tail. Mol Biol Cell. Biotechnol Adv. Cancer Res. Genes Cancer. Mol Cancer Ther. Nat Rev Cancer. J Intern Med. J Pathol. J Natl Cancer Inst. Sugimura T and Ushijima T: Genetic and epigenetic alterations in carcinogenesis. Mutat Res. Hum Genet. Cancer Biol Ther.

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  • Molecular Biology of Cancer Research Group.
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Institute of Molecular Biology and Tumor Research

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Cancer biology: Molecular and genetic basis - Oncology for Medical Students

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The Molecular Biology of Cancer The Molecular Biology of Cancer
The Molecular Biology of Cancer The Molecular Biology of Cancer
The Molecular Biology of Cancer The Molecular Biology of Cancer
The Molecular Biology of Cancer The Molecular Biology of Cancer
The Molecular Biology of Cancer The Molecular Biology of Cancer
The Molecular Biology of Cancer The Molecular Biology of Cancer
The Molecular Biology of Cancer The Molecular Biology of Cancer
The Molecular Biology of Cancer The Molecular Biology of Cancer
The Molecular Biology of Cancer

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